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M Driessens

Publications and source records attributed to M Driessens.

At least 19 recordsLinked to original sources
PubMed2002

Pseudodystrophy. A conversion disorder mimicking reflex sympathetic dystrophy.

The authors suggest some criteria by which pseudodystrophy and reflex sympathetic dystrophy, although sharing some similar clinical features, can be distinguished as two different conditions, each requiring its own approach and management. The most important distinction is found on bone scintigraphy. In reflex sympathetic dystrophy the bone scan shows a typical increased tracer uptake (at least during stages I and II); in pseudodystrophy there is a normal or decreased tracer uptake in the affected region. Moreover the vascularization is increased in reflex sympathetic dystrophy stage I, whereas in pseudodystrophy hypovascularization is found from the beginning. The clinical features, as well as the results of technical investigations, psychological evaluation and treatment of 4 patients with pseudodystrophy are presented. The importance of distinguishing this condition from reflex sympathetic dystrophy is stressed.

Adolescent↗
PubMed2001

Cdc42 induces filopodia by promoting the formation of an IRSp53:Mena complex.

BACKGROUND: The Rho GTPases Rho, Rac, and Cdc42 regulate the organization of the actin cytoskeleton by interacting with multiple, distinct downstream effector proteins. Cdc42 controls the formation of actin bundle-containing filopodia at the cellular periphery. The molecular mechanism for this remains as yet unclear. RESULTS: We report here that Cdc42 interacts with IRSp53/BAP2 alpha, an SH3 domain-containing scaffold protein, at a partial CRIB motif and that an N-terminal fragment of IRSp53 binds, via an intramolecular interaction, to the CRIB motif-containing central region. Overexpression of IRSp53 in fibroblasts leads to the formation of filopodia, and both this and Cdc42-induced filopodia are inhibited by expression of the N-terminal IRSp53 fragment. Using affinity chromatography, we have identified Mena, an Ena/VASP family member, as interacting with the SH3 domain of IRSp53. Mena and IRSp53 act synergistically to promote filopodia formation. CONCLUSION: We conclude that the interaction of Cdc42 with the partial CRIB motif of IRSp53 relieves an intramolecular, autoinhibitory interaction with the N terminus, allowing the recruitment of Mena to the IRSp53 SH3 domain. This IRSp53:Mena complex initiates actin filament assembly into filopodia.

3T3 Cells↗
PubMed2000

The mammalian homologue of the Caenorhabditis elegans polarity protein PAR-6 is a binding partner for the Rho GTPases Cdc42 and Rac1.

A mammalian homologue of the PDZ domain containing Caenorhabditis elegans protein PAR-6 was found in a yeast two-hybrid system screen as binding to the Rho family member Cdc42. PAR-6 contains a PDZ domain and in C. elegans it has been shown to be crucial for the asymmetric cleavage and establishment of cell polarity during the first cell divisions in the growing embryo. Mammalian PAR-6 interacted with Cdc42 and Rac1 both in the yeast two-hybrid system and in in vitro binding assays. Co-immunoprecipitation experiments, employing transiently transfected Cos-1 cells, further confirmed that Cdc42 and Rac1 are physiological binding partners for PAR-6. We found that, in epithelial Madin-Darby canine kidney cells (MDCK), endogenous PAR-6 was present in the tight junctions, as judged from its co-localisation with the tight junction protein ZO-1, however, PAR-6 was also detected in the cell nucleus. Stimulation of MDCK cells with scatter factor/hepatocyte growth factor induced a loss of PAR-6 from the areas of cell-cell contacts in conformity with their progressive breakdown. In C. elegans PAR-6 co-localises with PAR-3 and has been suggested to form a direct complex. In agreement with earlier studies, mammalian PAR-3 was found to be present in tight junctions of MDCK cells but, in contrast to PAR-6, the protein could not be detected in the nucleus. Furthermore, co-immunoprecipitation experiments, employing Cos-1 cells, demonstrated that mammalian PAR-6 and PAR-3 formed a direct complex. These findings, together with the reported roles of PAR-6 and PAR-3 in C. elegans, suggest that Cdc42 and Rac1 and PAR-6/PAR-3 are involved in the establishment of cell polarity in epithelial cells.

Animals↗
PubMed1999

What is reflex sympathetic dystrophy?

In the literature there is no unanimity with respect to the diagnosis of reflex sympathetic dystrophy (RSD). Frequently, the diagnosis is established on mere clinical grounds. In our opinion, however, bone scintigraphy is of major importance for the diagnosis. Using this examination, true RSD can be clearly differentiated from other conditions which are incorrectly diagnosed and treated as RSD. If the bone scan is not suggestive of RSD, the clinical picture, radiological examination and vascular scan may lead to the correct diagnosis. This may be a pseudodystrophy, in which a hypovascularization is found right from the start, while in true RSD there is initially a hypervascularization. Other conditions which may be confused with RSD are causalgia, neurotic compulsive postures, hysterical conversion, malingering and even self-mutilation. In the spontaneous course of RSD three phases can be distinguished. Stage I is the warm or hypertrophic phase, stage II the cold or atrophic phase. Per definition the third phase corresponds to stabilization or, in rare instances, to healing. By means of the vascular scan the correct stage can be determined, and the results of treatment evaluated. Finally it should be noted that in children the condition is completely different from true RSD, as it concerns a pseudodystrophy or disuse-related dystrophy. This condition may also be seen in adults and adolescents, usually females. The bone scan is always negative. In this way bone scintigraphy constitutes the means to answer the question as to what RSD is and what it is not. An algorithm for the differential diagnosis is presented.

Adolescent↗
PubMed1998

Activation of G1 progression, JNK mitogen-activated protein kinase, and actin filament assembly by the exchange factor FGD1.

Cdc42 has been shown to control bifurcating pathways leading to filopodia formation/G1 cell cycle progression and to JNK mitogen-activated protein kinase activation. To dissect these pathways further, the cellular effects induced by a Cdc42 guanine nucleotide exchange factor, FGD1, have been examined. All exchange factors acting on the Rho GTPase family have juxtaposed Dbl homology (DH) and pleckstrin homology (PH) domains. We report here that FGD1 triggers G1 cell cycle progression and filopodia formation in Swiss 3T3 fibroblasts as well as JNK mitogen-activated protein kinase activation in COS cell transfection assays. FGD1-induced filopodia formation is Cdc42-dependent, and both the DH and PH domains are essential. Although expression of the FGD1 DH domain alone does not activate Cdc42 and induce filopodia, it does trigger both the JNK cascade in COS cells and G1 progression in quiescent Swiss 3T3 cells. We conclude that FGD1 can trigger G1 progression independently of actin polymerization or integrin adhesion complex assembly. Furthermore, since FGD1 activates JNK and G1 progression in a Cdc42-independent manner, it must have additional, as yet unidentified, targets.

3T3 Cells↗
PubMed1997

Infrequent presentations of reflex sympathetic dystrophy and pseudodystrophy.

Pseudodystrophy is a condition that in the past was regarded incorrectly as a kind of reflex sympathetic dystrophy. The difference between both diseases can be ascertained easily by a bone scintigraphy. Other clinical features of pseudodystrophy are discussed. Infrequent presentations of reflex sympathetic dystrophy are described: radial, parcellar, and zonal cases; vertebral localization; and other misleading conditions.

Adolescent↗
PubMed1995

Hypogonadism as a cause of recurrent muscle injury in a high level soccer player. A case report.

Hypogonadotropic hypogonadism is a well known entity in highly trained female athletes. In male sportsmen, resting testosterone levels may be lowered especially in well endurance trained athletes and during high intensity training periods, frequently in combination with excessive weight reduction. However, only few reports illustrate a clinical pathology related to this state. In this report, where we present a case of a high level soccer player with recurrent muscle injuries over several years, hypogonadism was caused by sports activity together with an impaired testicular function (cryptorchidy). Clinical findings included testicular maldevelopment, decreased libido, infertility and a high incidence of muscle strains and delayed post-exercise soreness in mainly eccentric exercised muscle groups. Laboratory findings showed abnormally lowered resting testosterone values, most prominent during training periods, and an unfavourable testosterone/cortisol ratio during recuperation after exercise. With respect to treatment of the problem, neither any form of physical therapy nor rehabilitation program could give long lasting benefit. Using tamoxifen, an anti-oestrogenic drug, which stimulates LH and FSH production, we not only observed normal physiological resting testosterone values and a restoration of the testosterone/cortisol ratio after exercise, but our patient also experienced a higher sexual drive, well being and a spectacular decrease in the muscle injury rate. Although this patient was not a highly endurance trained athlete, we assume that a chronic anabolic/catabolic hormone imbalance may be of greater clinical importance in sports activity based on eccentric and explosive muscle work.

Adult↗
PubMed1991

The use of 99Tcm-HSA dynamic vascular examination in the staging and therapy monitoring of reflex sympathetic dystrophy.

Evaluation of the local haemodynamic changes was performed in 93 patients with untreated reflex sympathetic dystrophy, based upon a simple dynamic vascular examination technique, using 99Tcm-HSA. According to the disease stage, opposite observations were made: in stage I (n = 72) an increase in both blood flow and blood volume was found, in stage II (n = 21) in contrast, both blood flow and blood volume decreased. These findings show that reflex sympathetic dystrophy can be staged according to haemodynamic changes. It is obvious, moreover, that a careful haemodynamic staging is most important for the choice of the right vasoactive treatment; e.g. calcitonin (vasoconstrictive) versus guanethidine (vasodilating).

Calcitonin↗
PubMed1987

Clinical experience with cyclandelate in insulin-dependent diabetic patients with neuropathy.

Previous trials have demonstrated a clinical and electrophysiological improvement of diabetic peripheral polyneuropathy in diabetic patients treated with cyclandelate at a dosage of 1600 mg/day. Hence, a double-blind randomised trial was started in 16 insulin-dependent diabetic patients presenting with symptoms of neuropathy, an increased vibration perception threshold (VPT), disturbed tendon reflexes at lower limbs and an EMG showing a significantly decreased motor nerve conduction velocity (MCV) of the peroneal nerves. The placebo-treated group and the cyclandelate-treated group were not significantly different regarding age, duration of diabetes and level of metabolic control (measured as total HbA1), which remained unchanged during the year of observation. In the cyclandelate-treated group, pathological sensation improved significantly in 7 of 8 patients. MCV, measured under standardised conditions, increased significantly during the first 6 months of treatment, while mean VPT did not change. In the placebo group 3 of 8 patients showed an improvement of sensation, 3 did not feel any change and 2 worsened. Neither mean MCV nor VPT changed significantly. No severe side effects were observed during the study period.

Adult↗
PubMed1981

Effect of calcitonin, hydrocortisone, and parathyroid hormone on canine bone blood vessels.

Experiments were designed to determine whether or not calcitonin, parathormone, and glucocorticoids have direct effects on the vascular smooth muscle cells of bone blood vessels. Tibias of mongrel dogs were isolated. The arteria nutriens was cannulated and perfused at constant flow with aerated Krebs-Ringer solution (37 degrees C). The perfusion pressure was continuously recorded. In unstimulated preparations calcitonin caused dose-dependent increases in perfusion pressure, indicating that it causes constriction of bone blood vessels. Parathormone did not affect basal perfusion; it did not significantly alter vasoconstrictions caused by the injection of norepinephrine indicating that the hormone has no direct effect on the vascular smooth muscle of bone blood vessels. Hydrocortisone, at low concentrations, augmented the constrictions caused by exogenous norepinephrine and periarterial nerve stimulation; at higher concentrations, hydrocortisone caused a dose-dependent inhibition of the response to adrenergic activation. The depressant effect of hydrocortisone was antagonized by propranolol, suggesting that the glucocorticoid facilitates beta-adrenergic relaxation of the vascular smooth muscle cells by catecholamines.

Animals↗
PubMed1979

Vascular reactivity of the isolated tibia of the dog.

Experiments were performed to assess the responsiveness of vessels subserving bone tissue to nerve stimulation and to exogenously administered catecholamines and acetylcholine. Tibias of mongrel dogs were isolated and dissected free; the periosteum was left intact. The main nutrient artery was prepared and cannulated. Ring electrodes were placed around the artery. The preparation was perfused at constant flow with aerated (95% O2 - 5% CO2) Krebs-Ringer solution (37 degrees C) by means of a roller pump. The perfusion pressure was continuously recorded. For each preparation, the flow rate was used at which the response to a standard dose of norepinephrine was the largest. Periarterial electrical stimulation caused frequency-dependent increases in perfusion pressure; because these responses were blocked by phentolamine, they must be due to activation of sympathetic nerves. Injections of norepinephrine caused dose-dependent increases in perfusion pressure that were abolished by phentolamine. Acetylcholine caused dose-dependent, atropine-sensitive decrease of the constrictions caused by norepinephrine infusions. These experiments demonstrate that the isolated perfused tibia of the dog is a satisfactory preparation to investigate the direct effects of sympathetic nerve stimulation and naturally occurring vasoactive amines on bone blood vessels.

Acetylcholine↗
PubMedDate not supplied

[Peri-articular ossifications].

Restriction of motion of the joints due to peri-articular ossifications constitute a major problem in the rehabilitation of patients with transverse spinal cord lesion. The therapeutic possibilities as well as the preventive measurements are described and illustrated with a few case reports.

Adolescent↗